Effects Of Dietary Intervention On The Expression Of T-cadherin In The Liver Of Rats With NAFLD

Background and Aim: Non-alcoholic fatty liver disease(NAFLD) is a performance of metabolic syndrome in liver. Adiponectin is an adipokine that has anti-inflammtion,anti-diabetic and anti-atherosclerosis properties by binding to its receptors. Our preliminary research results indicated that the expression of adiponectin decreased in the liver from simple steatosis to NASH in the progression of NAFLD rats. T-cadherin is a new receptor of adiponectin. The purpose of this study is to investigate the role of T- cadherin in the pathogenesis of NAFLD rats, and the effect of diet intervention on the expression of T- cadherin.Methods: Forty male Sprague-Dawley rats were divided into five groups randomly, including two normal control groups(NC1 group: rats fed a normal diet for 8 weeks and NC2 group: rats fed a normal diet for 16 weeks), two HFD(high-fat diet) groups(HFD1 group: rats fed a high-fat diet for 8 weeks and HFD2 group: rats fed a high-fat diet for 16 weeks), and one dietary intervention group(DIET group: rats fed an HFD for 8 weeks and then switched to a normal diet for 8 weeks). The biochemical assays and serum adiponectin concentration were detected by ELISA. The protein expression of T-cadherin in the liver tissue was detected by immunohistochemical assay. T-cadherin m RNA expression in the liver was measured by RT-q PCR.Results: The NAS(Nonalcoholic fatty liver discase active score)of HFD1 group was significantly higher than NC1 group(3.7±0.52 vs 0.5±0.55,P<0.001); The NAS of HFD2 group were significantly higher than NC2 group(6.57±0.79 vs 0.5±0.54,P<0.001);The NAS of HFD2 group were significantly higher than HFD1 group(6.57±0.79 vs 3.70±0.52,P<0.001), reflecting the progression of NAFLD histology with prolonged time of high-fat diet. Compared with HFD2 group, the hepatic inflammation(0.86±0.38 vs 2.14±0.38, P<0.001)and steatosis(39.17±9.17 vs 82.14±6.98, P<0.001)of the DIET group decreased; In contrast to NC1 group, theprotein(6.53±0.57 vs 2.17±0.49, P<0.001) and mRNA(1.53±0.04 vs 1.00±0.1, P<0.05) expressions of T-cadherin in liver tissues increased in HFD1 group. In contrast to NC2 group, the protein(10.42±0.44 vs 2.58±0.43, P<0.001) and m RNA(3.09±0.15 vs 0.91±0.16, P<0.01) expressions of T-cadherin increased in HFD2 group. In contrast to HFD2 group, the protein(4.05±0.56 vs 10.42±0.44,P<0.001)and m RNA(1.38±0.04 vs 3.09±0.15,P<0.01)expressions of T-cadherin decreased in DIET group. The immunohistochemical scores of T-cadherin showed a positive correlation with the grade of hepatic inflammation(r=0.869,P<0.001), fat percentage(r=0.919,P<0.001)and ballooning degeneration(r=0.633,P<0.001).Conclusions: The high-fat diet can successfully establish the rat model of NAFLD. The hepatic expression of T-cadherin increased in the progression of NAFLD and decreased after the dietary intervention. The hepatic expression of T-cadherin was correlated positively with the grade of hepatic inflammation and fat percentage in NAFLD rats, suggesting that T-cadherin may be closely related to the pathogenesis of nonalcoholic fatty liver disease.